اثر نانوکورکومین خوراکی بر تشنج ناشی از پنتیلن تترازول داخل صفاقی و الگوی فسفوریلاسیون CaMKII در هیپوکامپ موش سوری نر
DOI::
https://doi.org/10.22100/jkh.v18i3.3061چکیده
مقدمه: مطالعات قبلی حاکی از آن است که تبدیل کورکومین به فرم نانو ذره می تواند موجب افزایش اثر درمانی آن در مدل های تشنج شود. نشان داده شده است که تغییرات پروتئین کیناز II وابسته به کلسیم/کالمودولین (CaMKII) با بعضی از مدل های تجربی صرع مرتبط است. مطالعه حاضر با هدف بررسی الگوی CaMKII هیپوکامپ متعاقب اثر درمانی نانوکورکومین در مدل تشنج ناشی از پنتیلن تترازول (PTZ) انجام گردید. مواد و روش ها: نانوکورکومین بر مبنای آلبومین سرم گاوی تولید شد و در دوزهای 50 و 100 میلی گرم/ کیلوگرم به صورت خوراکی(گاواژ) به موش های سوری نر نژاد NMRI با وزن 30-25 گرم تجویز گردید. یک ساعت بعد PTZ با دوز 85 میلیگرم/کیلوگرم به صورت داخل صفاقی به حیوان تجویز شد. متعاقب تزریق PTZ داخل صفاقی مدت زمان وقوع میوکلونوس، کلونوس، وقوع تشنج تونیک عمومی و میزان مرگ و میر در موشهای سوری نر ثبت گردید. پس از بررسی الگوی رفتاری تشنج ، حیوانات بیهوش شده کشته شدند و میزان فرمهای فسفریله و کامل CaMKII هیپوکامپ آنان از طریق روش وسترن بلات تعیین گردید. نتایج: نتایج نشان داد که تجویز خوراکی نانوکورکومین تولیدشده با BSA در دوزهای 50 و 100 میلی گرم بر کیلوگرم، در مقایسه با کورکومین طبیعی به طور قابل توجهی تشنج متعاقب PTZ را بهبود داد. در همه گروه ها تشنج موجب افزایش فسفوریلاسیون CaMKII هیپوکامپ شد و نانوکورکومین آن را تعدیل نکرد. نتیجه گیری: یافته های این مطالعه نشان داد که اثر درمانی نانوکورکومین در مدل تشنج ناشی از پنتیلن تترازول ارتباطی با تغییر الگوی فعالیت CaMKII هیپوکامپ ندارد.
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